title: [Research progress of the resistance mechanism of non-small cell lung cancer to EGFR-TKIs].
abstract: Nowadays, lung cancer is the malignant tumor of the highest morbidity and mortality over the world, and non-small cell lung cancer (NSCLC) makes up about 80%. There is a great many NSCLC patients have been in advanced stage when diagnosed. As a result, people pay more attention to curing advanced NSCLC. The standard treatment to advanced NSCLC is platinum-based combined chemotherapy. However, chemotherapy drugs usually have limited effects on improving the survival of the patients. Then exploring new therapies is extremely urgent to us. Now, molecular targeted therapy has been the most promising research area for the treatment of NSCLC with researches going deep into pathogenesis and biological behavior of lung cancer. Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have achieved a great success in the treatment of advanced NSCLC. Their representatives are erlotinib and gefitinib. The two drugs have been widely used to treat advanced NSCLCs worldwide, especially for the patients with EGFR activating mutations. However, after a period of treatment (median time is 6 to 12 months), most patients will develop drug resistance to EGFR-TKIs. Intense research in these NSCLCs has identified two major mechanisms of resistance to TKIs: primary and acquired resistances. The research about resistance mechanism of NSCLC to EGFR-TKIs is a hot one because of their excellent effects on improving overall and progression-free survival. The aim of this article was to summarize the development of the resistance mechanisms.
authors.affiliation: Department of Respiratory Medicine, Peking Union Medical College Hospital, Beijing 100730, China.
authors.forename: Huihui
authors.initials: H
authors.lastname: Liu
authors.forename: Mengzhao
authors.initials: M
authors.lastname: Wang
authors.forename: Ke
authors.initials: K
authors.lastname: Hu
authors.forename: Yan
authors.initials: Y
authors.lastname: Xu
authors.forename: Manjiao
authors.initials: M
authors.lastname: Ma
authors.forename: Wei
authors.initials: W
authors.lastname: Zhong
authors.forename: Jing
authors.initials: J
authors.lastname: Zhao
authors.forename: Longyun
authors.initials: L
authors.lastname: Li
authors.forename: Huazhu
authors.initials: H
authors.lastname: Wang
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy* / Q000235:genetics; D019008:Drug Resistance, Neoplasm; D066246:ErbB Receptors / Q000037:antagonists & inhibitors* / Q000235:genetics; D006801:Humans; D009154:Mutation; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*
chemical_list: D000970:Antineoplastic Agents; D047428:Protein Kinase Inhibitors; D066246:ErbB Receptors